Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)
Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)
The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)
Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)
Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)
Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

21. March 2010 William Davis (19)
No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

19. March 2010 William Davis (0)
If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)
In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)
If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)
No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.
All posts by william-davis

Let's make it a lot easier

24. February 2007 William Davis (0)
The American Heart Association just released a new set of consensus guidelines on heart disease prevention in women: Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update

For those of you following the Heart Scan Blog and the Track Your Plaque program, there will be little new in the guidelines. In fact, you'll wonder if the date on the front of the report should be 1987, rather than 2007. Did you know that you should exercise and eat healthy?

Take a look at the list of risk factors for coronary vascular disease (CVD) listed in the report:

Major risk factors for CVD, including:
Cigarette smoking
Poor diet
Physical inactivity
Obesity, especially central adiposity
Family history of premature CVD (CVD at <55>

Progress: You'll notice that buried inside the list is "Evidence of subclinical vascular disease (e.g., coronary calcification)". Just a few short years ago that wouldn't have even been included.

The Track Your Plaque contention is that, for the great majority of women, this list could be shortened to one item: coronary calcification. As time goes on, the people who argue and draft these guidelines will come to the realization that coronary calcification is the disease--it's not a risk for the disease, a predictor of the disease. Coronary calcification is the disease itself. The other items on the list recede way into the background when you know whether or not coronary atherosclerosis is present, i.e., you know your heart scan score (of coronary calcium).

The report goes to say such things as taking a little bit of fish oil is a good idea, maintaining a normal blood pressure is desirable. . . yada yada yada. You've heard this all before.

A major part of the treatment guidelines are devoted to LDL cholesterol reduction with statin agents. You shouldn't be surprised. It's amazing what $22 billion dollars in revenues will buy.

A closing paragraph reads:

'Population-wide strategies are necessary to combat the
pandemic of CVD in women, because individually tailored
interventions alone are likely insufficient to maximally prevent
and control CVD. Public policy as an intervention to
reduce gender-based disparities in CVD preventive care and
improve cardiovascular outcomes among women must become
an integral strategy to reduce the global burden of
CVD.'

Say that again? If you understood that bit of gobbledygook, you're a lot smarter than me.

Don't look to the American Heart Association report for any new ideas. It reminds me of the politician who reminds everybody of what a devoted family man he is: It has nothing to do with his policies. It just makes him look good. If compared to prior report, the 2007 report does indeed represent progress--but just oh so little.

No wonder nobody talks about real prevention

23. February 2007 William Davis (0)
Take a look at this eye-opening statement taken from a well-written NY Times article about Dr. Arthur Agatston, the South Beach Diet and now South Beach Heart Program books:


'We have made major improvements in prevention,” Dr. Gregg W. Stone, the director of cardiovascular research at Columbia University, says. “But it’s difficult. It takes frequent visits, a close relationship between a physician and a patient and a very committed patient.'

Which is exactly the atmosphere Dr. Agatston’s practice tries to create. Nurses there give patients specific cholesterol goals to meet and help them deal with the side effects of the drugs they are taking. A nutritionist, Marie Almon, meets with patients frequently enough to discuss real-life issues like how to stick to a high-fiber Mediterranean diet even on a cruise or a business trip.

There is only one problem with this shining example of a medical practice: it is losing money.


From NY Times, January 24, 2007. What’s a Pound of Prevention Really Worth? (Find the full text at http://www.nytimes.com/2007/01/24/business/24leonhardt.html?ex=1172379600&en=4268a738e82857da&ei=5070.)

It gets at one of the fundamental reasons why your cardiologist will probably never talk to you about an intense approach to prevention: it doesn't pay. Because John Q. Cardiologist focuses, instead, on how to increase procedural volume, train how to put in the next best defibrillator, etc., there is little consciousness about preventive issues. Just the simple matter of taking fish oil causes their eyes to glaze over.

That's why the Track Your Plaque program exists: it is a portal for the kind of information you cannot get. Of course, you could read all the scientific studies, attempt years of trial and error, and try to gain a sense of how to do this yourself. Or you could follow this program. We are proud to not worry about generating procedural profits. We ar unbiased by drug or medical device money. We say exactly what we mean.

By the way, we are on a current push to really "beef-up" our online discussions via real-time chat. Long-term, we'd like to be able to offer chat with our staff many hours every day. Be patient. It will happen, but not today.

HDL and vitamin D

22. February 2007 William Davis (5)
I know of no published reports on this question, but I've now seen numerous people experience significant jumps in HDL with raising blood vitamin D to 25-OH-vitamin D3.

Last week, for example, I had a man who had struggled with raising HDL from a starting level of 28 mg/dl. On niacin, exercise, weight loss, fish oil, red wine, and cilostazol (a prescription agent that I use occasionally that raises HDL), his HDL rose to 41 mg/dl--better, but hardly to our goal.

I added vitamin D, 4000 units, and raised his 25-OH-vitamin D3 level from 22 ng/ml to 53 ng/ml. Next HDL: 73 mg/dl! Small LDL improves along with a rise in HDL.

Not everybody's response is this dramatic. I see more typical rises of 5 to 10 mg/dl every day. I'm uncertain of why the response is inconsistent, though people who begin with lower vitamin D levels seem to experience a larger HDL increase. I wonder if the partial normalization of insulin and glucose responses is at work, or some anti-inflammatory effect.

Vitamin D provides so many other benefits, as well as HDL-raising. I hope you've gone to the effort to have your blood level checked to determine your replacement need. If not, now's the time. February represents your nadir (lowest point) for 25-OH-vitamin D3 blood levels.

Even more Michael Pollan

20. February 2007 William Davis (0)
"Eat food. Not too much. Mostly plants.

That, more or less, is the short answer to the supposedly incredibly complicated and confusing question of what we humans should eat in order to be maximally healthy. I hate to give away the game right here at the beginning of a long essay, and I confess that I’m tempted to complicate matters in the interest of keeping things going for a few thousand more words. I’ll try to resist but will go ahead and add a couple more details to flesh out the advice. Like: A little meat won’t kill you, though it’s better approached as a side dish than as a main. And you’re much better off eating whole fresh foods than processed food products. That’s what I mean by the recommendation to eat “food.” Once, food was all you could eat, but today there are lots of other edible foodlike substances in the supermarket. These novel products of food science often come in packages festooned with health claims, which brings me to a related rule of thumb: if you’re concerned about your health, you should probably avoid food products that make health claims. Why? Because a health claim on a food product is a good indication that it’s not really food, and food is what you want to eat."

Michael Pollan, author of my latest favorite book, The Omnivore's Dilemma, wrote a wonderful piece for the New York Times entitled "Unhappy Meals". You can find the full text at http://www.nytimes.com/2007/01/28/magazine/28nutritionism.t.html?ex=1172120400&en=a78c20f4da0cdc7b&ei=5070. (Another favorite read of mine, The Fanatic Cook's Blog at , alerted me to Pollan's article. Incidentally, take a look at the Fanatic Cook's latest posts--very entertaining and informative. She's got incisive insight into foods as well as a great sense of humor.)

Pollan goes on to say that...

"...typical real food has more trouble competing under the rules of nutritionism, if only because something like a banana or an avocado can’t easily change its nutritional stripes (though rest assured the genetic engineers are hard at work on the problem). So far, at least, you can’t put oat bran in a banana. So depending on the reigning nutritional orthodoxy, the avocado might be either a high-fat food to be avoided (Old Think) or a food high in monounsaturated fat to be embraced (New Think). The fate of each whole food rises and falls with every change in the nutritional weather, while the processed foods are simply reformulated. That’s why when the Atkins mania hit the food industry, bread and pasta were given a quick redesign (dialing back the carbs; boosting the protein), while the poor unreconstructed potatoes and carrots were left out in the cold.

Of course it’s also a lot easier to slap a health claim on a box of sugary cereal than on a potato or carrot, with the perverse result that the most healthful foods in the supermarket sit there quietly in the produce section, silent as stroke victims, while a few aisles over, the Cocoa Puffs and Lucky Charms are screaming about their newfound whole-grain goodness."

Not everything Pollan says is new, but he says it so eloquently and cleverly that he's worth reading. If you haven't yet read Omnivore's Dilemma, or just want a condensed version of the book, the New York Times piece is a great piece of the world according to Michael Pollan.

My life is easy

17. February 2007 William Davis (3)
In the old days (the 1980s and 1990s), practicing cardiology was very physically and emotionally demanding. Since procedures dominated the practice and preventive strategies were limited, heart attacks were painfully common. It wasn't unusual to have to go to the hospital for a patient having a heart attack at 3 am several times a week.

Those were the old days. Nowadays, my life is easy. Heart attacks, for the most part, are a thing of the past in the group of people who follow the Track Your Plaque principles. I can't remember the last time I had a coronary emergency for someone following the program.

But I am reminded of what life used to be like for me when I occasionally have to live up to my hospital responsibilities and/or cover the practices of my colleagues. (Though I voice my views on prevention to my colleagues, the most I get is a odd look. When a colleague recently covered my practice for a weekend while I visited family out of town, he commented to me how quiet my practice was. I responded, "That's because my patients are essentially cured." "Oh, sure they are." He laughed. No registration that he had witnessed something that was genuine and different from his experience of day-to-day catastrophe among his own patients. None.)

I recently had to provide coverage for a colleague for a week while he took his family to Florida. During the 7 days, his patients experienced 4 heart attacks. That is, 4 heart attacks among patients under the care of a cardiologist.

If you want some proof of the power of prevention, watch your results and compare them to the "control" group of people around you: neighbors, colleagues, etc. Unfortunately, the word on prevention, particularly one as powerful as Track Your Plaque, is simply not as widespread as it should be. Instead, it's drowned out in the relentless flood of hospital marketing for glitzy hospital heart programs, the "ask your doctor about" ads for drugs like Plavix, which is little better than spit in preventing heart attacks (except in stented patients), and the media's fascinating with high-tech laser, transplant, robotic surgery, etc.

Prevention? That's not news. But it sure can make the slow but sure difference between life and death, having a heart attack or never having a heart attack.

My bread contains 900 mg omega-3

15. February 2007 William Davis (8)
Phyllis is the survivor of a large heart attack (an "anterior" myocardial infarction involving the crucial front of the heart) several years ago. Excessive fatigue prompted a stress test, which showed poor blood flow in areas outside the heart attack zone. This prompted a heart catheterization, then a bypass operation one year ago.

FINALLY, Phyllis began to understand that her unhealthy lifestyle played a role in causing her heart disease. But lifestyle alone wasn't to blame. Along with being 70 lbs overweight and overindulging in unhealthy sweets every day, she also had lipoprotein(a), small LDL particles, and high triglycerides. The high triglycerides were also associated with its evil "friends," VLDL and IDL (post-prandial, or after-eating, particles).

When I met her, Phyllis' triglycerides typically ranged from 200-300 mg/dl . Fish oil was the first solution, since it is marvelously effective for reducing triglycerides, as well as VLDL and IDL. Her dose: 6000 mg of a standard 1000 mg capsule (6 capsules) to provide 1800 mg EPA + DHA, the effective omega-3 fatty acids.

But Phyllis is not terribly good at following advice. She likes to wander off and follow her own path. She noticed that the healthy bread sold at the grocery store and containing flaxseed boasted "900 mg of omega-3s per slice!". So she ate two slices of the flaxseed-containing bread per day and dropped the fish oil.

Guess what? Triglycerides promptly rebounded to 290 mg/dl, along with oodles of VLDL and IDL.

A more obvious example occurs in people with a disorder called "familial hypertriglyceridemia," or the inherited inability to clear triglycerides from the blood. These people have triglycerides of 800 mg/dl, 2000 mg/dl, or higher. Fish oil yields dramatic drops of hundreds, or even thousands of mg. Fish oil likely achieves this effect by activating the enzyme, lipoprotein lipase, that is responsible for clearing blood triglycerides. Flaxseed oil and other linolenic acid sources yield . . .nothing.

Don't get me wrong. Flaxseed is a great food. As the ground seed, it reduces LDL cholesterol, reduces blood sugar, provides fiber for colon health, and may even yield anti-cancer benefits. Flaxseed oil is a wonderful oil, rich in monounsaturates, low in saturates, and rich in linolenic acid, an oil fraction that may provides heart benefits a la Mediterranean diet.

But linolenic acid from flaxseed is not the same as EPA + DHA from fish oil. This is most graphically proven by the lack of any triglyceride-reducing effects of flaxseed preparations.

Enjoy your flaxseed oil and ground flaxseed--but don't stop your fish oil because of it. Heart disease and coronary plaque are serious business. You need serious tools to combat and control them. Fish oil is serious business for triglycerides. Flaxseed is not.

More Omnivore's Dilemma

11. February 2007 William Davis (2)
Another irresistible quote from Michael Pollan’s book, The Omnivore’s Dilemma:

“In many ways breakfast cereal is the prototypical processed food: four cents’ worth of commodity corn (or some other equally cheap grain) transformed into four dollars’ worth of processed food. What an alchemy! Yet it is performed straightforwardly enough: by taking several of the output streams issuing from a wet mill (corn meal, corn starch, corn sweetener, as well as a handful of tinier chemical fractions) and then assembling them into an attractively novel form. Further value is added in the form of color and taste, then branding and packaging. Oh yes, and vitamins and minerals, which are added to give the product a sheen of healthfulness and to replace the nutrients that are lost whenever whole foods are processed. On the strength of this alchemy the cereals group generates higher profits for General Mills than any other division. Since the raw materials in processed foods are so abundant and cheap (ADM and Cargill will gladly sell them to all comers) protecting whatever is special about the value you add to them is imperative.”

A food manufacturer’s nightmare is when you and your family shop in the produce aisle in the grocery store. Produce is unmodified (aside from the pesticide and genetic-engineering issues), not added to, and therefore of no interest to the food manufacturer, since no additional profit can be squeezed out of it. If you pay 45 cents for a cucumber, there’s no room for a processor to multiply it’s return.

Vegetables and fruits have imperfections, no doubt, particularly pesticide residues and the “dumbing-down” of some foods to increase their desirability (e.g., green grapes, what I call “grape candy”). But vegetables and fruits are the closest you can get to foods that are essentially unmodified by a food manufacturer. Due to the absence of processing, they are not calorie-dense like a bag of chips; they include all the naturally-occurring healthy factors like flavonoids that food scientists have, thus far, struggled and failed to identify, quantify, and control; and they lack all the unhealthy additives that processed foods require for extended shelf life, palatability, and reconstitution (anti-separating agents, emulsifiers, sweeteners, etc.)

Vegetables, in particular, should be the cornerstone of your plaque control program. Not breakfast cereals, breads, bacon, sausage, mayonnaise, fruit drinks and soda, all the foods that worsen the causes of coronary plaque and raise your heart scan score.

If you would like to understand how the current perverted state of affairs in food have come about, Pollan’s book is must reading.

Pollan's The Omnivore's Dilemma

11. February 2007 William Davis (0)

“ ‘You are what you eat’ is a truism hard to argue with, and yet it is, as a visit to a feedlot suggests, incomplete, for you are what what you eat eats, too. And what we are, or have become, is not just meat but number 2 corn and oil.”

Author Michael Pollan offers unique, enlightening, and entertaining insights into the food we eat in his new book, The Omnivore’s Dilemma: A natural history of four meals.

Pollan draws parallels between the dilemma of the primitive human living in the wild, having to stumble through the choices of animals and plants that could nourish or kill, and the ironically modern return of this phenomenon in present-day supermarkets. While the dangers of food choices aren’t as immediate as in the wild (eat the wrong mushroom or herb, for instance, and you die), they can nonetheless be life-threatening, or at least health-threatening. Hydrogenated oils, high-fructose corn syrup, carageenan, guar gum. . .“What is all this stuff anyway, and where in the world did it come from?”

Among the issues Pollan discusses is that of modern cattle raising practices: the rush to fatten a cow from an 80 lb calf to a 1200-pound, bloated cow over a period of 14 months. Nature created this animal to mature over a 4 to 5 year period through grazing, thus it’s beautifully “engineered” ruminant system that allows it to digest cellulose in grasses, a process that humans and other mammals are incapable of. The pressures to bring greater quantities of beef to market at a reduced price and make more money have resulted in a farming industry that encourages the incorporation of unnatural, often inhumane practices like corn feeding (rather than grass grazing), refeeding of bovine body parts (thus “mad cow disease”), and widespread and chronic administration of hormones and antibiotics.

(I can't help but think that the rapid and perverse fattening of cattle by industrial "farming" is paralleled by the fattening of the eating American. After all, we are the hapless recipients of this flood of cheap, unhealthy, plasticized food.)

The industrialization of food has de-personalized the act of eating. You no longer have any connection with the green pepper in your salad (unless you grew it yourself), nor do you have any appreciation for the suffering of the cow in your hamburger. Worse, the distortion of livestock raising practices has modified the food composition of meat. Range-fed animals, leaner and richer in omega-3 fatty acids, have been replaced by the marbled, saturated fat-rich modern grocery bought meats.

This is a theme that Pollan reiterates time and again: how food processing adds value to the manufacturer, often starting with a healthy ingredient but modifying it, adding ingredients, taking out others, until it’s something decidedly unhealthy. Yet the manufacturer will trumpet the fact that a healthy ingredient is included. Breakfast cereals are the most blatant example of this. What the heck are Cheerios but an over-processed attempt to make more money out of the simple oat?

Pollan’s eloquent and unique insights into food are definitely worth reading.

As always, per our Track Your Plaque policy, I recommend Mr. Pollan’s book strictly on its merits. We obtain no “cut”, commission, or other financial gain by recommending his book. Track Your Plaque members pay their modest membership fee for truth. They do not pay for us to advertise something that provides hidden advantage to us. We do not advertise, editorialize to steer you towards a specific product or service. What we say, we truly believe.

The most frequently asked question of all

8. February 2007 William Davis (0)
The most frequently asked question on the Track Your Plaque website:

"Can you recommend a doctor in my area who can help me follow the Track Your Plaque program?"

This is a problem. Unfortunately, I wish I could tell everyone that we have hundreds or thousands of physicians nationwide who have been thoroughly educated and adhere to the principles I believe are crucial in heart disease:

1) Identify and quantify the amount of coronary atherosclerotic plaque present. In 2007, the best technique remains CT heart scans.

2) Identify all hidden causes of plaque. This includes Lp(a), post-prandial disorders, small LDL, and vitamin D deficiency.

3) Correct all patterns.


But we don't.

You'd think that this simple formula, as straightforward and rational as it sounds, would be easily followed by many if not most physicians. But Track Your Plaque followers know that it simply is not true. My colleagues, the cardiologists, are hell-bent on implanting the next new device, providing a lot more excitement to them as well as considerably more revenue.

The primary care physician is already swamped in a sea of new information, going from osteoporosis drugs, to arthritis, to gynecologic issues, to skin rashes and flu. Heart disease prevention? Oh yeah, that too. They can only dabble in heart disease prevention a la prescription for Lipitor. That's quick and easy.

Nonetheless, I believe we should work towards identifying the occasional physician who is indeed willing to help people follow a program like Track Your Plaque. As we grow, we will need to identify some mechanism of professional education and we will maintain a record of these practitioners. But right now, we're simply already stretched to the limit just doing what we are doing.

If you come across a physician who practices in this fashion and you've had a positive relationship, we'd like to hear about it.

Do stents kill?

6. February 2007 William Davis (5)
There's apparently a lively conversation going on at the HeartHawk Blog (www.hearthawk.blogspot.com). Among the hot topics raised was just how bad it is to have a stent.

I think that my comments some time back may have started this controversy. I've lately noticed that having a stent screws up your heart scan scoring in the vicinity of the stent. I was referring to the fact that I've now seen several people in the Track Your Plaque program do everything right and then show what I call "regional reversal": unstented arteries show dramatic drops in score of 18-30%, but the artery with a stent shows significant increase in score.

This is consistent with what we observe in the world outside Track Your Plaque when stents are inserted. Someone will get a stent, for instance, in the left anterior descending artery. A year later, there will be a "new" plaque at the mouth of the stent or just beyond the far end. This is generally treated by inserting another stent. Use of a drug-coated stent seems to have no effect on this issue.

Now, my smart friends in the Track Your Plaque program would immediately ask, "Does this mean you continually end up chasing these plaques that arise as a result of stents? Do you create an endless loop of procedures?"

Thankfully, the majority of times you do not. Rarely, this does happen and can lead to need for bypass surgery to circumvent the response. But it is unusual. The tissue that grows above and below stents does seem to be unusually impervious to the preventive efforts we institute.

Perhaps there's some new supplement, medication, or other strategy that will address this curious new brand of plaque growth. Until then, you and I can only take advantage of what is known. If it's any consolation, the plaque that seems to grow because of a previously inserted stent seems to lack the plaque "rupture" capacity of "naturally-occuring" plaque. It is, indeed, somehow different. It is more benign, less likely to cause heart attack. It's always been my feeling that this tissue behaves more like the "scar" tissue that grows within stents, causing "re-stenosis", a more benign, less rupture-prone kind of tissue.